Dexmedetomidine Injection into the Locus Ceruleus Produces Antinociception

Abstract

Part of the mechanism by which dexmedetomidine produces an antinociceptive effect is by an action directly on the LC, demonstrated by these studies in which antinociception produced by injection of this drug into the LC can be blocked by specific alpha(2) antagonists injected into the LC. Furthermore, the action of dexmedetomidine in the LC in turn may result in an increase in activation of alpha(2) adrenoceptors in the spinal cord, because the antinociceptive effect of LC dexmedetomidine injection also can be blocked by intrathecal injection of antipamezole and pertussis toxin.

Epidural Dexmedetomidine and Clonidine as a adjunct with Bupivacaine in patients undergoing lower limb orthopedic Surgeries. A Clinical Study.

“…[28], [29], [30] The results of our study clearly indicate the effectiveness of epidural dexmedetomidine as adjuvant to bupivacaine in providing sedation, more patients in Group A had sedation score 3 and were arousable by gentle tactile stimulation as compared to Group B. Similar results were seen in study done by.…”

Substitution of a mutant α 2a -adrenergic receptor via “hit and run” gene targeting reveals the role of this subtype in sedative, analgesic, and anesthetic-sparing responses in vivo

“…The LC has been implicated in the sedative effect of ␣ 2 AR agonists (33), and the analgesic response to ␣ 2 AR agonists occurs via both supraspinal (including the LC) and spinal loci (36,44,45). Our studies indicate that mutation of the ␣ 2A AR eliminates sedative-hypnotic as well as analgesic responses to ␣ 2 AR agonists without causing a general perturbation of the neural system because other non-␣ 2 AR-directed agents produce expected physiological and electrophysiological responses.…”

“…The LC is the site for expression of ␣ 2 AR-mediated, sedative-hypnotic responses (33,34) and participates in ␣ 2 ARinduced analgesic effect (35,36). In situ hybridization in the mouse brain has revealed dense ␣ 2A AR localization in the LC (31), thus facilitating electrical detection of ␣ 2A AR-expressing neurons.…”

O uso de dexmedetomidina na sedação de crises hipercianóticas em um recém-nascido com tetralogia de Fallot

“…Activation of α2-adrenoreceptors in the central nervous system, particularly in the locus ceruleus, is involved in the sedative action of dexmedetomidine by reducing central sympathetic flow. 10 Because the α2-agonist should have little direct effect on respiration, based on receptor binding studies, the effects of dexmedetomidine on respiratory function can be minimal. 10,11 Previous reports on the clinical use of this agent in pediatric patients are generally consistent with these pharmacologic profiles, demonstrating that dexmedetomidine provided profound sedation levels without significant adverse effects on ventilation.…”

“…10 Because the α2-agonist should have little direct effect on respiration, based on receptor binding studies, the effects of dexmedetomidine on respiratory function can be minimal. 10,11 Previous reports on the clinical use of this agent in pediatric patients are generally consistent with these pharmacologic profiles, demonstrating that dexmedetomidine provided profound sedation levels without significant adverse effects on ventilation. 12 In adult cases, however, respiratory complications have been reported, which are mostly associated with large and rapid initial loading doses.…”